|Molar mass||865.36 g mol−1|
|Appearance||off white powder|
|Melting point||45.6 C|
|Solubility in water||practically insoluble in water|
| (what is: / ?)
Except where noted otherwise, data are given for materials in their standard state (at 25 °C or 77 °F, 100 kPa)
Ubiquinol is an electron-rich (reduced) form of coenzyme Q10.
The natural ubiquinol form of coenzyme Q10 is 2,3-dimethoxy-5-methyl-6-poly prenyl-1,4-benzoquinol, where the polyprenylated side chain is 9-10 units long in mammals. Coenzyme Q10 (CoQ10) exists in three redox states, fully oxidized (ubiquinone), partially reduced (semiquinone or ubisemiquinone), and fully reduced (ubiquinol). The redox functions of ubiquinol in cellular energy production and antioxidant protection are based on the ability to exchange two electrons in a redox cycle between ubiquinol (reduced) and the ubiquinone (oxidized) form.
Ubiquinol is a lipid-soluble benzoquinol that is found in all cellular systems and in nearly every cell, tissue, and organ in mammals. Ubiquinol is acquired through biosynthesis, supplementation, and in small amounts from diet. Ubiquinol has an established role as an essential component of the electron transport chain transferring electrons resulting in ATP synthesis. In mammals ATP production takes place predominantly in mitochondria and to a lesser extent in other organelles such as the Golgi apparatus or endoplasmic reticulum. The mitochondria typically produce nearly 95% of the energy required for cellular growth, development, and healthy metabolism. The antioxidant action of ubiquinol is now considered to be one of the most important functions in cellular systems.
Ubiquinol is a potent lipophilic antioxidant capable of regenerating other antioxidants such as tocopherol (Vitamin E) and ascorbate (Vitamin C). Recent studies have also revealed its function in gene expression involved in human cell signaling, metabolism, and transport.
- 1 Nutrient function summary
- 2 Energy production
- 3 Cardiovascular effects
- 4 Antioxidant effects and aging
- 5 Neuronal health
- 6 Oral health
- 7 Renal health
- 8 Male Infertility
- 9 Inflammation and gene expression
- 10 Other findings
- 11 Bioavailability
- 12 Content in foods
- 13 Molecular aspects
- 14 References
- 15 External links
Nutrient function summary
Ubiquinol is the antioxidant form of CoQ10 and is essential for mitochondrial synthesis of energy. It is the only known lipid-soluble antioxidant that is endogenously synthesized, protecting biological membranes against lipid peroxidation as well as regenerating other antioxidants such as Vitamin C and Vitamin E. Published clinical and experimental research shows that ubiquinol affects cardiovascular health, neuronal metabolism, renal health, and genes related to lipid / lipoprotein metabolism and inflammation.
In terms of its functions, ubiquinol's primary roles are in the synthesis of mitochondrial energy and as a protective antioxidant. The vitamin-like nutrient is found concentrated in the inner mitochondrial membrane where it serves as a carrier of reducing equivalents in the mitochondrial electron transport chain’s I and II complexes toward complex III. In this process, ubiquinol serves to produce ATP (adenosine triphosphate), the main energy intermediate in living organisms.
The effects of ubiquinone (oxidized, spent form) and ubiquinol (antioxidant form) have been studied on heart failure patients. The subjects in the study were classified as having NYHA Class IV congestive heart failure and being on maximal medical therapy. The patients were being administered a mean amount of 450 mg ubiquinone per day. Their blood levels of CoQ10 ranged from 0.9 to 2.0 µg/mL plasma (mean value of 1.4 µg/mL), an amount that the researcher considered subtherapeutic. Subjects were then switched over to 450 mg ubiquinol per day, and the follow up data from six of the subjects showed mean blood values of CoQ10 rose from 1.4 µg/mL to 4.1 µg/mL. In addition to the significant increase in plasma CoQ10, ejection fraction increased nearly twofold from 24% to 45%. The ejection fraction is an assessment method that measures the ability of the heart’s ventricles to pump blood. While many factors can impact the ejection fraction including gender and method utilized for calculation, the typical healthy adult exhibits an ejection fraction of 60-65%. Additionally, beneficial effects in heart function could be demonstrated clinically, as subjects had an average improvement from NYHA Class IV to Class II. Based upon the recent clinical experience by Dr. Langsjoen, the therapeutic plasma CoQ10 levels are now considered to be > 3.5 μg/ml, which is a significantly higher blood value than the > 2.5 μg/ml target in the past. In this study, there were no adverse effects of ubiquinone or ubiquinol, nor any drug interaction including patients on coumadin.
In 2010, researchers from Germany’s University of Kiel and Japan’s Shinshu University published a study examining genome-expression effects of ubiquinol and ubiquinone in an experimental model utilizing SAMP1 (Senescence Accelerated Mice Prone 1) mice. After 14 months of supplementation, the mice liver tissue was analyzed for a variety of gene expressions via microarray testing. The gene expression profiling demonstrated a functional connection between ubiquinol and the following signaling pathways: PPAR-α, LXR/RXR, and FXR/RXR. In all, eleven different ubiquinol-dependent genes related to cholesterol and lipid or lipoprotein metabolism were identified. With the exception of one gene, ubiquinone did not have any effect on these genes.
The mevalonate pathway (also known as the HMG-CoA reductase pathway) is an important metabolic pathway responsible for producing a diverse array of cellular products, including cholesterol and CoQ10 forms ubiquinone and ubiquinol. Statin medication targets inhibition of the mevalonate pathway to decrease cholesterol biosynthesis, however a consequence of their utilization is a depletion of CoQ10. Statins do not block all cholesterol production in the body. Similarly CoQ10 levels are not lowered completely. Nevertheless even a slight drop in CoQ10 levels can have a host of effects, some of which are not evident for years or even decades. The most common adverse effect of statins is skeletal muscle toxicity (myopathy), and the clinical manifestation of myopathy varies widely ranging from mild myalgia to rhabdomyolysis. Researchers recently investigated the effects of ubiquinol in 28 patients with statin myopathy. Nine subjects received atorvastatin, six subjects received rosuvastatin, six subjects received simvastatin, three subjects received fluvastatin, two subjects received lovastatin, and one patient received pravastatin. After 6 months of supplementation with 60 mg of ubiquinol per day, there was a significant reduction in muscle pain and weakness: muscle pain declined by 53.8% (p<0.0001) and muscle weakness declined by 44% (p<0.0001). The scientists noted that a limitation of the study was the heterogenous statin medication.
In another recent ubiquinol study published in the European Journal of Pharmacology, researchers have investigated the effects of statins on mitochondrial biosynthesis and oxidative metabolism in muscle tissue. The in vitro experiment utilized human rhabdomyosarcoma cells, which are cells commonly implemented in studies for making inferences about muscle tissue adaptation. Specifically, the researchers sought to determine the effect of simvastatin treatment (at concentrations of 0.5 or 1.0 μM) on various metabolic markers, and to assess the impact of concurrent administration of simvastatin and ubiquinol. Simvastatin treatment suppressed basal oxidative metabolism in a dose dependent manner. The suppression of oxidative metabolism was rescued by concurrent treatment with ubiquinol (0.5 or 1.0 μM). Cells treated with simvastatin demonstrated a significant decline in ATP content, and this negative circumstance was rescued in a dose-dependent manner by concurrent administration of ubiquinol. PGC-1α levels were also significantly reduced by simvastatin at a concentration of 0.5 μM at time point 48 hours. The biomarker PGC-1α is of particular interest in bioenergetic research because it is considered the master regulator of mitochondrial biogenesis, and is also a powerful stimulator of Sirtuin 3 gene expression. The simultaneous treatment with ubiquinol (0.5 and 1.0 μM concentrations) rescued the simvastatin-induced decline in PGC-1α. The scientists also demonstrated that treatment with simvastatin significantly reduced mitochondrial content and cell viability, which were both rescued by simultaneous administration with ubiquinol. These findings, according to the scientists, provide fundamental in vitro evidence that statins may reduce metabolic capacity in muscles, which can be rescued by ubiquinol administration.
Antioxidant effects and aging
Ubiquinol is a potent lipid-soluble antioxidant capable of regenerating alpha tocopherol. It is important because it is the only lipid soluble antioxidant synthesized in the body. CoQ10 scientists have been investigating the relationship between suboptimal states marked by high levels of oxidative stress and the relative levels of ubiquinone and ubiquinol in the body - - both of which combined comprise a value called "total CoQ10". Disorders marked by elevated oxidative stress can cause major changes to the amounts of ubiquinol and ubiquinone in the body, a factor that is referred to by scientists as the ratio of ubiquinol to ubiquinone (ubiquinol:ubiquinone). Another way to describe this is through ubiquinol ratio, which is the percentage of ubiquinol in the total amount of CoQ10. A profound change was noted in the CoQ10 profile of type II diabetic subjects. Specifically, there was a decrease in the plasma ubiquinol ratio, suggesting a surge in oxidative stress. Another study also showed loss of ubiquinol in conditions marked by elevated oxidative stress. Subjects with hepatitis, cirrhosis, and hepatoma all exhibited a decrease in the ubiquinol concentrations, while the levels of total CoQ10 (ubiquinol + ubiquinone) was not reduced.
Some preliminary information indicates that ubiquinol may be involved in the aging process, as scientists have evaluated the ubiquinone and ubiquinol blood levels in subjects of different age groups. Not only do aged subjects have reduced CoQ10 biosynthesis, their ability to convert ubiquinone to ubiquinol is also diminished. The specific alignment of ubiquinol was recently investigated by creating unilamellar vesicles containing ubiquinol to probe the antioxidant’s position in cellular membranes. Based on the fluorescence exposure to the vesicles, the scientists concluded that ubiquinol distributes closer to the cell membrane surface rather than the interior hydrophobic region of the membranes.
A collaborative study between Waseda University and Tsukuba University demonstrated beneficial effects of ubiquinol on middle-aged and elderly women (average of 63.7 years of age). Following an eight-week period of supplementation with 150 mg ubiquinol per day, subjects displayed significant improvements in physical activity and mental health scores (as measured by daily step count and SF-36 health survey).
A number of small studies have shown CoQ10 to benefit the neurological system, which includes the brain. In 2002, a study was published which examined the effects of CoQ10 (ubiquinone) in patients with early Parkinson's disease. The scientists in that multi-center effort (Phase II study, funded by the National Institute of Neurological Disorders and Stroke [NINDS]) found that ubiquinone reduced the functional decline in Parkinson's disease.
In light of the favorable results, a large, multi-center FDA NIH-approved Phase III study is currently underway.
Another study took a comparative look at the protective effects of ubiquinone and ubiquinol in rodents administered MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine), a neurotoxin that induces changes similar to those found in idiopathic Parkinson’s disease.
MPTP is selectively toxic to cells of the substantia nigra, which are specialized cells in the brain stem involved in motor control and dopamine neurotransmitter synthesis. While both forms offered protection again MTPT-induced toxicity, ubiquinol exerted a stronger effect.
Oral health comprises all aspects of the mouth, including the teeth and gums (gingiva) and their connective tissue, lips, tongue, and salivary glands. Emerging scientific information continues to establish a relationship between oral health status and a variety of systemic conditions, ranging from diabetes, respiratory diseases, osteoporosis, arthritis, and cardiovascular diseases. Oral health and systemic health are part of a bidirectional interface (each capable of exerting an effect on the other), and the link between the two is inflammation. Orally, inflammation may commonly be found in the condition known as periodontitis, which may result in the destruction of tooth-supporting collagen, alveolar bone, and the teeth. Periodontitis is known to elevate systemic markers of inflammation, such as C-reactive protein (an acute phase protein synthesized in the liver) and serum neutrophil elastase.
Researchers from the University of Sevilla in Spain identified that subjects with periodontitis had elevated mitochondrial ROS and significantly reduced coenzyme Q10 levels than subjects without periodontitis (60.2 pmol /mg protein versus 150.4 pmol Q, indicating a decline of 56%). A primary pathogenic factor giving rise to periodontal inflammation is the excess generation of reactive oxygen species (ROS). These ROS are leaked by the mitochondria as a by-product of the energy synthesis process.
While coenzyme Q10 is essential for mitochondrial synthesis of energy, it may also counter ROS formation, provided the coenzyme Q10 is in the ubiquinol form. Ubiquinol has specifically been shown to exert potent anti-inflammatory effects as seen in a genoexpression study involving human immune cells (monocytic cells known as THP-1). In that research model, the human immune cells were exposed to bacterial cell wall lipopolysaccharide (LPS) to induce expression and secretion of proinflammatory cytokines. Ubiquinol caused a reduction in the cellular release of various proinflammatory substances, specifically cytokine TNF-α and two chemokines.
The ubiquinol form of coenzyme Q10 has been studied specifically for its impact on oral health. Results were presented in June 2011 at the 63rd Meeting of the Vitamin Society of Japan by Nihon University School of Dentistry by researchers evaluating the effects of 150 mg of ubiquinol per day over a two-month period in a double-blind, placebo-controlled clinical trial. The scientists measured various indicators of periodontal health including plaque adhesion, pocket depth, bleeding, and gingival recession. Ubiquinol demonstrated significant benefits in plaque adhesion and an increase in the salivary antioxidant status, which are essential for the maintenance of oral health. A possible mechanism of these oral benefits may be based on the antioxidant effect of ubiquinol, which could counteract periodontal inflammatory processes.
One factor that affects oral health is the amount of salivary secretion. Insufficient salivary secretion, also known as xerostomia, is associated with several negative effects including increased susceptibility to dental caries and periodontal disease. A comparative study by Japanese researchers examined the effects of ubiquinol and ubiquinone on salivary secretion. Sixty-six patients were given either ubiquinol or ubiquinone at a dosage of 100 mg per day, or a placebo over a one month period. While both forms of orally administered coenzyme Q10 significantly enhanced salivary coenzyme Q10 levels, the ubiquinol form provided the greater rise in concentration: ubiquinone levels elevated from 60 to 87 ng/mL while ubiquinol elevated from 54.6 to 117.7 ng/mL. In addition, ubiquinol stimulated greater salivary secretion thus solidifying its position as the optimum form of coenzyme Q10 for oral health.
Nevertheless, no serious review article has until this day proven any clinical or otherwise therapeutical effects of coenzyme Q10 on periodontal disease or any other oral disease.
Researchers from the University of Tokyo have been examining the role of antioxidants in Chronic kidney disease. As a preliminary study, an animal model of chronic kidney disease was developed. Three experimental groups were created: a control group, a high salt diet group, and a high salt diet plus ubiquinol group. In comparison to the control group, the high salt diet increased oxidative stress (measured by the generation of superoxide anion in kidney tissue), increased hypertension, and induced albuminuria. However, the high salt diet plus ubiquinol group exhibited results indicating significant renoprotection by ubiquinol, including decreased generation of superoxide anion (antioxidant effect), decreased urinary albumin, and amelioration of hypertension. This study marks the first experimental research with the antioxidant ubiquinol in an animal model of chronic kidney disease.
A recent study published in 2012 in a peer-reviewed publication The Journal of Urology investigated the effects of the ubiquinol (reduced form of CoQ10 or CoQ10H2) in subjects with male infertility. A total of 228 men participated in the double-blind, placebo controlled, randomized clinical trial over a 26-week treatment period. Subjects in the study had the male infertility condition known as idiopathic oligoasthenoteratozoospermia (OAT), which is marked by poor semen quality criteria with less than 14% normal forms, oligozoospermia by a sperm concentration of less than 20 X 106 spermatozoa per ml and asthenozoospermia by less than 50% of motile spermatozoa with forward progression according to WHO criteria.
|Parameter measured||Ubiquinol (200 mg/day)||Placebo|
|Sperm volume and density||
|Seminal plasma AOX CAT-like activity||
|Seminal plasma AOX-SOD-like activity||
The study results demonstrated that supplementation with 200 mg of ubiquinol per day significantly improved sperm density, sperm motility, and sperm strict morphology. The researchers pointed out that oxidative stress (OS) is one of the main factors that influence male infertility, and that OS is known to negatively affect the ubiquinol-to-ubiquinone ratio.
Inflammation and gene expression
Scientists have initiated a series of studies to examine the effects of CoQ10 on gene expression. In silico analysis of hundreds of genes have revealed CoQ10 to affect 17 different genes, which are functionally connected by four different cellular signalling pathways: G-protein coupled receptors, KAK/STAT, integrin, and beta-arrestin. Researchers involved in that study subsequently performed detailed investigations with the ubiquinol form. An in vitro investigation utilizing a human monocyte cell line (THP-1) exposed to a stimulator of inflammation called lipopolysaccharide (LPS) showed ubiquinol inhibited the release of proinflammatory substances, specifically cytokine TNF-α pro-inflammatory chemokines RANTES (normal T-call expressed and secreted) and MIP1-α (macrophage inflammatory protein). The scientists observed ubiquinol to exert a stronger effect on these inflammation-mediators than ubiquinone.
Further research along these lines demonstrate some of these genes related to the inflammation process to be redox-sensitive. An in-vivo study was conducted utilizing both ubiquinone or ubiquinol on an accelerated aging rodent model strain called SAMP1. A variety of different tissues (liver, heart, brain, and kidney) were analyzed through microarray-based whole genomic expression profile. One of the findings was that ubiquinol was more effective than ubiquinone in raising CoQ10 levels in the liver (this effect of greater bioavailability has also been observed in humans). A review of the genome expression profiles on the liver samples revealed a ubiquinol-specific effect for genes in the PPAR-α (peroxisome proliferator activated receptor alpha) signaling pathway. Interestingly, these ubiquinol-sensitive genes are primarily involved in cholesterol synthesis (for example, 3-hydroxy-3-methylglutaryl-coenzyme A), lipid metabolism (FABP5), and lipoprotein metabolism (PLTP). These effects were specific for ubiquinol, as the regulation of PPAR-α genes was not observed with ubiquinone.
One study examined the relationship between ubiquinol and blood lipids in patients with Coronary Artery Disease. Specifically, the scientists sought to determine if a relationship exists between the extent of stenosis (narrowing of blood vessels) and the concentrations of ubiquinol and blood lipids. Often, CoQ10 is studied in relation to blood lipids, since in the blood it is almost entirely found in lipoproteins (in particular low-density lipoprotein cholesterol LDL-C). In turn, lipoproteins package lipid soluble cholesterol for circulation in the water soluble blood (cholesterol is not found free), and hence the association between CoQ10, cholesterol, and lipoproteins. The subjects were not administered any ubiquinol or statins, thus providing a point of differentiation from other studies where supplementation took place. In order to quantify the extent of stenosis, the subjects underwent coronary angiography. Of the 36 total subjects, 20 were qualified as negative (less than 50% stenosis) while 16 subjects were positive (greater than 70% stenosis). The findings revealed the ubiquinol / lipids ratio was significantly higher in the low-stenosis group; conversely, the high-stenosis group had significantly lower values of the ubiquinol / lipids ratio. The scientists remarked that the ubiquinol / lipid ratio appears to be a sensitive factor for marking the progress of atherosclerotic changes. While this was not an intervention trial, an association did emerge between the ubiquinol / lipids ratio and the extent of stenosis.
It is well established that CoQ10 is not well absorbed into the body, as has been published in many peer-reviewed scientific journals. Since the ubiquinol form has two additional hydrogens, it results in the conversion of two ketone groups into hydroxyl groups on the active portion of the molecule. This causes an increase in the polarity of the CoQ10 molecule and may be a significant factor behind the observed enhanced bioavailability of ubiquinol.
Orally, ubiquinol exhibits greater bioavailability than ubiquinone: 150 mg per day of ubiquinol in a softgel resulted in peak blood values of 3.84 µg/ml within 28 days.
However, there are authorities that dispute whether ubiquinol is more bioavailble in practice rather then in theory compared to CoQ10 supplements because those have their CoQ10 molecules dissolved in lipid micelles which then deliver their cargo to the plasma membrane in the intestinal wall. There they dissolve via simple diffusion in the intestinal cells, then onto the lymph vessels, and then into the venous system. Since ubiquinol and CoQ10 are redox pairs and can and are rapidly inter-converted in the body it is not clear that ubiqinol's more hydrophilic nature compared to CoQ10 is of practical significance. 
Content in foods
In foods, there are varying amounts of ubiquinol. An analysis of a range of foods found ubiquinol to be present in 66 out of 70 items and accounted for 46% of the total coenzyme Q10 intake. The following chart is a sample of the results.
|Food||Ubiquinol (μg/g)||Ubiquinone (μg/g)|
The reduction of ubiquinone to ubiquinol occurs in Complexes I & II in the electron transfer chain. The Q cycle is a process that occurs in cytochrome b, a component of Complex III in the electron transport chain, and that converts ubiquinol to ubiquinone in a cyclic fashion. When ubiquinol binds to cytochrome b, the pKa of the phenolic group decreases so that the proton ionizes and the phenoxide anion is formed.
If the phenoxide oxygen is oxidized, the semiquinone is formed with the unpaired electron being located on the ring.
A page on Proteopedia, Complex III of Electron Transport Chain, contains rotatable 3-D structures of Complex III which may be used to study the peptide structures of Complex III and the mechanism of the Q cycle.
- Mellors, A; Tappel, AL (1966). "The inhibition of mitochondrial peroxidation by ubiquinone and ubiquinol". The Journal of Biological Chemistry 241 (19): 4353–6. PMID 5922959.
- Mellors, A.; Tappel, A. L. (1966). "Quinones and quinols as inhibitors of lipid peroxidation". Lipids 1 (4): 282–4. doi:10.1007/BF02531617. PMID 17805631.
- Battino, Maurizio; Ferri, Elida; Gorini, Antonella; Villa, Roberto Federico; Huertas, Jesus Francisco Rodriguez; Fiorella, Pierluigi; Genova, Maria Luisa; Lenaz, Giorgio et al. (1990). "Natural Distribution and Occurrence of Coenzyme Q Homologues". Molecular Membrane Biology 9 (3): 179–90. doi:10.3109/09687689009025839. PMID 2135303.
- Green, David E.; Tzagoloff, Alexander (1966). "The mitochondrial electron transfer chain". Archives of Biochemistry and Biophysics 116 (1): 293–304. doi:10.1016/0003-9861(66)90036-1. PMID 4289862.
- Frei, Balz; Kim, Mike C.; Ames, Bruce N. (1990). "Ubiquinol-10 is an Effective Lipid-Soluble Antioxidant at Physiological Concentrations". Proceedings of the National Academy of Sciences of the United States of America 87 (12): 4879–83. Bibcode:1990PNAS...87.4879F. doi:10.1073/pnas.87.12.4879. JSTOR 2354427. PMC 54222. PMID 2352956.
- Arroyo, A.; Navarro, F.; Navas, P.; Villalba, J. M. (1998). "Ubiquinol regeneration by plasma membrane ubiquinone reductase". Protoplasma 205: 107–13. doi:10.1007/BF01279300.
- Langsjoen, Peter H.; Langsjoen, Alena M. (2008). "Supplemental ubiquinol in patients with advanced congestive heart failure". BioFactors 32 (1–4): 119–28. doi:10.1002/biof.5520320114. PMID 19096107.
- Langsjoen, Peter H; Langsjoen, Alena M (27–30 May 2010). "Supplemental Ubiquinol in congestive heart failure: 3 year experience". 6th International Coenzyme Q10 Conference Brussels. pp. 29–30.
- Schmelzer, Constance; Okun, Jürgen G.; Haas, Dorothea; Higuchi, Keiichi; Sawashita, Jinko; Mori, Masayuki; Döring, Frank (2010). "The reduced form of coenzyme Q10 mediates distinct effects on cholesterol metabolism at the transcriptional and metabolite level in SAMP1 mice". IUBMB Life 62 (11): 812–8. doi:10.1002/iub.388. PMID 21086475.
- Feng, Qiping; Wilke, Russell A; Baye, Tesfaye M (2012). "Individualized risk for statin-induced myopathy: Current knowledge, emerging challenges and potential solutions". Pharmacogenomics 13 (5): 579–94. doi:10.2217/pgs.12.11. PMC 3337775. PMID 22462750.
- Zlatohlavek, L; Vrablik, M; Grauova, B; Motykova, E; Ceska, R (2012). "The effect of coenzyme Q10 in statin myopathy". Neuro endocrinology letters. 33 Suppl 2: 98–101. PMID 23183519.
- Vaughan, Roger A.; Garcia-Smith, Randi; Bisoffi, Marco; Conn, Carole A.; Trujillo, Kristina A. (2013). "Ubiquinol rescues simvastatin-suppression of mitochondrial content, function and metabolism: Implications for statin-induced rhabdomyolysis". European Journal of Pharmacology 711 (1–3): 1–9. doi:10.1016/j.ejphar.2013.04.009. PMID 23624330.
- Navas, Plácido; Villalba, José Manuel; De Cabo, Rafael (2007). "The importance of plasma membrane coenzyme Q in aging and stress responses". Mitochondrion 7: S34–40. doi:10.1016/j.mito.2007.02.010. PMID 17482527.
- Lim, S. C.; Tan, H. H.; Goh, S. K.; Subramaniam, T.; Sum, C. F.; Tan, I. K.; Lee, B. L.; Ong, C. N. (2006). "Oxidative burden in prediabetic and diabetic individuals: Evidence from plasma coenzyme Q10". Diabetic Medicine 23 (12): 1344–9. doi:10.1111/j.1464-5491.2006.01996.x. PMID 17116186.
- Yamamoto, Yorihiro; Yamashita, Satoshi (1999). "Plasma ubiquinone to ubiquinol ratio in patients with hepatitis, cirrhosis, and hepatoma, and in patients treated with percutaneous transluminal coronary reperfusion". BioFactors 9 (2–4): 241–6. doi:10.1002/biof.5520090219. PMID 10416036.
- Wada, Hiroo; Goto, Hajime; Hagiwara, Shin-Ichi; Yamamoto, Yorihiro (2007). "Redox Status of Coenzyme Q10 is Associated with Chronological Age". Journal of the American Geriatrics Society 55 (7): 1141–2. doi:10.1111/j.1532-5415.2007.01209.x. PMID 17608895.
- Fiorini, Rosamaria; Ragni, Letizia; Ambrosi, Simona; Littarru, Gian Paolo; Gratton, Enrico; Hazlett, Theodore (2007). "Fluorescence Studies of the Interactions of Ubiquinol-10 with Liposomes". Photochemistry and Photobiology 84 (1): 209–14. doi:10.1111/j.1751-1097.2007.00221.x. PMID 18173722.
- Shimizu, K, et al. (November 6th and 7th, 2010). "Collaborative research with Waseda University and Tsukuba University". The 21st Annual Meeting of Japanese Society of Clinical Sports Medicine. Tsukuba International Congress Center, Tsukuba, Ibraki Prefecture, Japan.
- Shults, C. W.; Oakes, D; Kieburtz, K; Beal, MF; Haas, R; Plumb, S; Juncos, JL; Nutt, J et al. (2002). "Effects of Coenzyme Q10 in Early Parkinson Disease: Evidence of Slowing of the Functional Decline". Archives of Neurology 59 (10): 1541–50. doi:10.1001/archneur.59.10.1541. PMID 12374491.
- Cleren, Carine; Yang, Lichuan; Lorenzo, Beverly; Calingasan, Noel Y.; Schomer, Andrew; Sireci, Anthony; Wille, Elizabeth J.; Beal, M. Flint (2008). "Therapeutic effects of coenzyme Q10 (CoQ10) and reduced CoQ10 in the MPTP model of Parkinsonism". Journal of Neurochemistry 104 (6): 1613–21. doi:10.1111/j.1471-4159.2007.05097.x. PMID 17973981.
- Kuo, Lan-Chen; Polson, Alan M.; Kang, Taeheon (2008). "Associations between periodontal diseases and systemic diseases: A review of the inter-relationships and interactions with diabetes, respiratory diseases, cardiovascular diseases and osteoporosis". Public Health 122 (4): 417–33. doi:10.1016/j.puhe.2007.07.004. PMID 18028967.
- Wohlfeil, Martin; Wehner, Jasmin; Schacher, Beate; Oremek, Gerhard M.; Sauer-Eppel, Hildegund; Eickholz, Peter (2009). "Degree of gingivitis correlates to systemic inflammation parameters". Clinica Chimica Acta 401 (1–2): 105–9. doi:10.1016/j.cca.2008.11.017. PMID 19061879.
- Bullon, Pedro; Cordero, Mario David; Quiles, José Luis; Morillo, Juan Manuel; Ramirez-Tortosa, Maria del Carmen; Battino, Maurizio (2011). "Mitochondrial dysfunction promoted by Porphyromonas gingivalis lipopolysaccharide as a possible link between cardiovascular disease and periodontitis". Free Radical Biology and Medicine 50 (10): 1336–43. doi:10.1016/j.freeradbiomed.2011.02.018. PMID 21354301.
- Prakash, Shobha; Sunitha, J; Hans, Mayank (2010). "Role of coenzyme Q10as an antioxidant and bioenergizer in periodontal diseases". Indian Journal of Pharmacology 42 (6): 334–7. doi:10.4103/0253-7613.71884. PMC 2991687. PMID 21189900.
- Schmelzer, Constance; Lorenz, Gerti; Rimbach, Gerald; Döring, Frank (2009). "In Vitro Effects of the Reduced Form of Coenzyme Q10 on Secretion Levels of TNF-α and Chemokines in Response to LPS in the Human Monocytic Cell Line THP-1". Journal of Clinical Biochemistry and Nutrition 44 (1): 62–6. doi:10.3164/jcbn.08-182. PMC 2613501. PMID 19177190.
- Sugano, N, et al. (June 4th and 5th, 2011). "Research by Nihon University School of Dentistry". The Sixty-third Meeting of the Vitamin Society of Japan. Hiroshima, Japan.
- Ryo, Koufuchi; Ito, Atsuko; Takatori, Rie; Tai, Yoshinori; Arikawa, Kazumune; Seido, Taro; Yamada, Takashi; Shinpo, Keiko et al. (2011). "Effects of coenzyme Q10 on salivary secretion". Clinical Biochemistry 44 (8–9): 669–74. doi:10.1016/j.clinbiochem.2011.03.029. PMID 21406193.
- Ishikawa, Akira; Kawarazaki, Hiroo; Ando, Katsuyuki; Fujita, Megumi; Fujita, Toshiro; Homma, Yukio (2010). "Renal preservation effect of ubiquinol, the reduced form of coenzyme Q10". Clinical and Experimental Nephrology 15 (1): 30–3. doi:10.1007/s10157-010-0350-8. PMID 20878200.
- Safarinejad, Mohammad Reza; Safarinejad, Shiva; Shafiei, Nayyer; Safarinejad, Saba (2012). "Effects of the Reduced Form of Coenzyme Q10 (Ubiquinol) on Semen Parameters in Men with Idiopathic Infertility: A Double-Blind, Placebo Controlled, Randomized Study". The Journal of Urology 188 (2): 526–31. doi:10.1016/j.juro.2012.03.131. PMID 22704112.
- Döring, Frank; Schmelzer, Constance; Lindner, Inka; Vock, Christina; Fujii, Kenji (2007). "Functional connections and pathways of coenzyme Q10-inducible genes: An in-silico study". IUBMB Life 59 (10): 628–633. doi:10.1080/15216540701545991. PMID 17852568.
- Schmelzer, Constance; Kubo, Hiroshi; Mori, Masayuki; Sawashita, Jinko; Kitano, Mitsuaki; Hosoe, Kazunori; Boomgaarden, Inka; Döring, Frank et al. (2009). "Supplementation with the reduced form of Coenzyme Q10 decelerates phenotypic characteristics of senescence and induces a peroxisome proliferator-activated receptor-α gene expression signature in SAMP1 mice". Molecular Nutrition & Food Research 54 (6): 805. doi:10.1002/mnfr.200900155.
- Miles, Michael V. (2007). "The uptake and distribution of coenzyme Q(10)". Mitochondrion 7: S72–7. doi:10.1016/j.mito.2007.02.012. PMID 17446143.
- Žáková, Pavla; Kanďár, Roman; Škarydová, Lucie; Skalický, Jiří; Myjavec, Andrej; Vojtíšek, Petr (2007). "Ubiquinol-10/lipids ratios in consecutive patients with different angiographic findings". Clinica Chimica Acta 380 (1–2): 133–8. doi:10.1016/j.cca.2007.01.025. PMID 17336955.
- James, Andrew M.; Cochemé, Helena M.; Smith, Robin A. J.; Murphy, Michael P. (2005). "Interactions of Mitochondria-targeted and Untargeted Ubiquinones with the Mitochondrial Respiratory Chain and Reactive Oxygen Species: Implications for the use of exogenous ubiquinones as therapies and experimental tools". Journal of Biological Chemistry 280 (22): 21295–312. doi:10.1074/jbc.M501527200. PMID 15788391.
- Hosoe, Kazunori; Kitano, Mitsuaki; Kishida, Hideyuki; Kubo, Hiroshi; Fujii, Kenji; Kitahara, Mikio (2007). "Study on safety and bioavailability of ubiquinol (Kaneka QH™) after single and 4-week multiple oral administration to healthy volunteers". Regulatory Toxicology and Pharmacology 47 (1): 19–28. doi:10.1016/j.yrtph.2006.07.001. PMID 16919858.
- Judy, William. "Coenzyme Q10 Facts or Fiction". Thorne Research. Retrieved 9 December 2013.
- Kubo, Hiroshi; Fujii, Kenji; Kawabe, Taizo; Matsumoto, Shuka; Kishida, Hideyuki; Hosoe, Kazunori (2008). "Food content of ubiquinol-10 and ubiquinone-10 in the Japanese diet". Journal of Food Composition and Analysis 21 (3): 199–210. doi:10.1016/j.jfca.2007.10.003.
- Slater, E.C. (1983). "The Q cycle, an ubiquitous mechanism of electron transfer". Trends in Biochemical Sciences 8 (7): 239–42. doi:10.1016/0968-0004(83)90348-1.
- Trumpower BL (June 1990). "Cytochrome bc1 complexes of microorganisms". Microbiol. Rev. 54 (2): 101–29. PMC 372766. PMID 2163487.
- Trumpower, Bernard L. (1990). "The Protonmotive Q Cycle". The Journal of Biological Chemistry 265 (20): 11409–12. PMID 2164001.
- http://proteopedia.org/wiki/index.php/Complex_III_of_Electron_Transport_Chain[full citation needed][unreliable medical source?]